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At least 865 records · Page 48Linked to original sources
PubMed1993

Argon laser scatter photocoagulation in treatment of branch retinal vein occlusion. A prospective clinical trial.

The objective of this prospective study was to ascertain whether scatter argon laser photocoagulation to the involved sector in major branch retinal vein occlusion and ischemic hemicentral retinal vein occlusion (a) prevents development of retinal and/or optic disk neovascularization and vitreous hemorrhage, and (b) affects visual acuity, visual fields and macular retinal lesions. The study was done in 271 eyes allocated to either treated (n = 61 eyes) or untreated (n = 210) groups. In this study, on an average follow-up of 3.6 years, the laser treatment (1) significantly reduced the risk of development of retinal neovascularization and vitreous hemorrhage, (2) did not affect the visual acuity and macular retinal lesions, and (3) produced a significant worsening in the peripheral visual fields compared to the untreated eyes. In view of our findings, we recommend that argon laser photocoagulation treatment should be given only when neovascularization is seen and not otherwise, because in the latter case, its detrimental effects may outweigh its beneficial ones.

Aged↗
PubMed2006

Ocular neovascularization: Implication of endogenous angiogenic inhibitors and potential therapy.

Ocular neovascularization (NV) is the primary cause of blindness in a wide range of ocular diseases, such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). The exact mechanism underlying the pathogenesis of ocular NV is not yet well understood, and as a consequence, there is no satisfactory therapy for ocular NV. In the last 10 years, a number of studies provided increasing evidence demonstrating that the imbalance between angiogenic stimulating factors and angiogenic inhibitors is a major contributor to the angiogenesis induced by various insults, such as hypoxia or ischemia, inflammation and tumor. The angiogenic inhibitors alone or in combination with other existing therapies are, therefore, believed to be promising in the treatment of ocular NV in the near future. This article reviews recent progress in studies on the mechanisms and treatment of ocular NV, focusing on the implication and therapeutic potential of endogenous angiogenic inhibitors in ocular NV.

Angiogenesis Inhibitors↗
PubMedDate not supplied

Ocular neovascularization: an epidemiologic review.

Neovascularization occurs in many eye diseases, and its epidemiologic impact is significant. However, data on the prevalence and incidence of ocular neovascularization have never been compiled to demonstrate its pervasiveness. This overview of ocular angiogenesis provides a review of the epidemiologic literature for neovascularization in various parts of the eye, including the cornea, iris, retina, and choroid. Relevant disease states are reviewed, as are their risk factors, so that their pathogenesis can be better understood. Data on the prevalence and incidence of the major diseases involving angiogenesis are synthesized to provide statistical evidence of the span and magnitude of ocular neovascularization. These prevalence and incidence data on ocular neovascularization are extrapolated to USA population data where possible, and "worst-case" estimates are calculated as well. Information was gathered with a search of the MEDLINE database, published monographs and volumes, and consultation with a number of primary authors. This study attempts to unify much of past and present epidemiologic research, and the information is presented in sections divided according to the anatomy of the eye.

Choroid↗
PubMed2000

Choroideremia associated with subretinal neovascular membrane.

PURPOSE: To report two Japanese patients with choroideremia, one male and one heterozygous female, who developed subretinal neovascular membrane and/or subretinal fibrosis in the intermediate stage of the disease, and, in addition, to describe marked clinical manifestation in a heterozygous carrier female. METHOD: Two patients were examined by slip-lamp biomicroscopy, ophthalmoscopy and other ophthalmoloscopic examinations. RESULTS: Two cases showed moderately advanced ophthalmoscopic and functional abnormalitities compatible with choroideremia, and in addition, subretinal lesion in the fovea and/or midperiphery. CONCLUSION: The intermediate stage of choroideremia may occasionally be complicated with choroidal neovascular membrane in the fovea, the midperiphery, or both, which resolves spontaneously and results in subretinal fibrous scarring. The occurrence of this complication in the fovea leads to episodic central visual loss, while midperipheral lesion may remain unrecognized.

Adolescent↗
PubMed1998

[Subretinal neovascular membranes in membranoproliferative glomerulonephritis type II].

BACKGROUND: So called 'dense deposits' in the retina of a patient suffering from membranoproliferative glomerulonephritis type II (MPGN II) were first demonstrated in 1989. Appearence of subretinal neovascular membranes associated with MPGN II in three patients was described in 1990. PATIENT AND METHODS: We present a 45-year-old male patient, whose insufficiency of the kidney due to a membranoproliferative glomerulonephritis type II required peritoneal dialysis and later transplantation. In both eyes fundus examination revealed typical disseminated, partly confluencing, drusen-like 'dense deposits' and exsudative degeneration of the macula due to subretinal neovascular membranes. Visual acuity was less than 20/400 and visual fields were reduced to small excentrics islands. There was an atrophy of the optic nerve with nearly extinguished VEP in both eyes. CONCLUSION: Flecked changes of the retina called 'dense deposits' associated with membranoproliferative glomerulonephritis type II have to be differentiated in particular from drusen, as well as metabolic-toxic and degenerative retinopathy. Development of subretinal neovascular membranes is attributed to altered retinal pigment epithelium, similar to age-related macular degeneration. An atrophy of the optic nerve associated with this disease has not been described so far. It is possible that vascular damage because of hypertensive changes due to renal dysfunction is the reason for the optic nerve atrophy. With another hypothesis this could be caused by intraocular pressure due to a risen flow of water into the vitreous cavity following the altered osmotic gradient after peritoneal dialysis.

Cell Membrane↗
PubMed1975

Retinal venous sheathing and neovascularization in disseminated sclerosis.

A 54-year-old black woman with no significant visual complaint and a diagnosis of disseminated sclerosis of 18 years' duration is presented because of marked bilateral sheathing of the retinal veins, and previously unreported dilated collateral vessels and early neovasularization secondary to peripheral vein occlusion.

Collateral Circulation↗
PubMed1996

Inhibition of vascular endothelial growth factor prevents retinal ischemia-associated iris neovascularization in a nonhuman primate.

OBJECTIVE: To determine if the angiogenic peptide vascular endothelial growth factor (VEGF) is required for retinal ischemia-associated iris neovascularization in a nonhuman primate. METHODS: Laser retinal vein occlusion was used to produce retinal ischemia in 16 eyes of eight animals (Macaca fascicularis). Eyes were randomized to treatment every other day with intravitreal injections of either a neutralizing anti-VEGF monoclonal antibody or a control monoclonal antibody of the same isotype. Serial iris fluorescein angiograms were assessed using a standardized grading system and masked readers. Retinal VEGF and placental growth factor expression were assessed by Northern blotting. The specificity of the antibodies was determined in capillary endothelial cell proliferation assays prior to intravitreal injection. RESULTS: Zero of eight eyes receiving the neutralizing anti-VEGF antibodies developed iris neovascularization. Five of eight control antibody-treated eyes developed iris neovascularization. The difference was statistically significant (P = .03). Intravitreal antibody injection did not impair the ability of the ischemic retina to increase VEGF messenger RNA expression. The anti-VEGF antibodies specifically inhibited VEGF-driven capillary endothelial cell proliferation in vitro. CONCLUSION: These data demonstrate that VEGF is required for iris neovascularization in an adult nonhuman primate eye. The inhibition of VEGF is a new potential therapeutic strategy for the treatment of ocular neovascularization.

Animals↗
PubMed1992

[Quantitative computerized image analysis of the relationship between neovascularization and nonperfusion area in branch retinal vein occlusion].

Quantitative computerized image analysis of composite fluorescein angiograms of 62 eyes with branch retinal vein occlusion (BRVO) found 33 eyes with newly formed blood vessels. Determination of the ratio of the retinal capillary nonperfusion area to the disk area revealed that the ratio was positively correlated with the incidence of neovascularization, in that 10.0% of the cases with the ratio under 10 and 63.2% of the cases with the ratio between 10-30 had neovascularization, and the incidence of the latter increased to 82.6% among cases with the ratio over 30. The calibres of 344 retinal arteries and veins in normal subjects and in the affected and unaffected eyes of BRVO patients were measured to find that both vessels were narrowed in late patients of retinal vein occlusion.

Fluorescein Angiography↗
PubMed1996

Retinitis pigmentosa with recurrent vitreous hemorrhage.

We observed recurrent vitreous hemorrhage in two patients with retinitis pigmentosa: a 41-year-old female and a 49-year-old male. At age 41, the first patient had diffuse capillary dilatation, macular microaneurysms, and paramacular macroaneurysms in the right eye. At age 47, similar retinal vascular lesions and disc neovascularization developed in the left eye followed by recurrent vitreous hemorrhage. The retinal microvascular changes and vitreous hemorrhages subsided spontaneously during the ensuring 4 years. In the second case, recurrent vitreous hemorrhage developed in the right eye. Funduscopy and fluorescein angiography at age 49 revealed no angiopathy. However, 2 years later we detected retinal neovascularization in the macula and an avascularity in the peripheral retina in the right eye. Subretinal exudate or retinal detachment was consistently absent in both cases.

Adult↗
PubMed1985

Irradiation of the posterior ocular segment with the neodymium-YAG laser in its free-running mode.

A neodymium-YAG laser, operating in its free-running mode with pulse durations of 10 to 20 ms, was used to treat 63 cases of choroidal and retinal diseases. These cases included diabetic background retinopathies, thrombosis of the central retinal vein or branch retinal vein, neovascular membranes under the pigment epithelium, and retinal breaks or degenerations of the peripheral retina. Because the number of diabetic retinopathies (24) and their average follow-up time (25.5 months) are insufficient for the evaluation of irradiation effects, no definite statement as to the merits of this energy modality in such cases can be made. The irradiation of infarcted retina was followed by extensive atrophy of the involved area. No secondary glaucoma was observed during a follow-up period of 16.4 months. The irradiation in four cases of neovascular subretinal membranes was followed by disappearance of the membranes. However, relapse later occurred in all four cases. The irradiation of eight retinal breaks resulted in solid scar tissue. Two choroidal melanomas were destroyed and did not recur during a follow-up period of 22 months.

Choroid↗
PubMed2005

Inhibition of ocular neovascularization by hedgehog blockade.

Ocular neovascularization associated with proliferative diabetic retinopathy and age-related macular degeneration is the leading cause of severe visual loss in adults in developed countries. Physiological and pathological retinal angiogenesis may occur independently in postnatal life through the complex activation of pro- and antiangiogenic pathways. We report that the Sonic hedgehog (Shh) pathway is activated in the retina in animal models of retinal and choroidal neovascularization. We show that pharmacological inhibition of the Shh signaling pathway significantly reduces physiological retinal angiogenesis and inhibits pathological vascularization in both models. Under retinal hypoxic conditions, inhibition of the Shh pathway results in reduction of vascular endothelial growth factor (VEGF) level, along with that of Patched-1 (Ptch1), a canonical Shh target, thus placing Shh activation upstream of VEGF in experimental retinal neovascularization. Our data demonstrate the requirement of the Shh pathway for retinal angiogenesis and its inhibition as a potential therapeutic strategy targeting ocular neovascular disease.

Animals↗
PubMed2001

Intrachoroidal neovascularization in transgenic mice overexpressing vascular endothelial growth factor in the retinal pigment epithelium.

Choroidal neovascularization in age-related macular degeneration is a frequent and poorly treatable cause of vision loss in elderly Caucasians. This choroidal neovascularization has been associated with the expression of vascular endothelial growth factor (VEGF). In current animal models choroidal neovascularization is induced by subretinal injection of growth factors or vectors encoding growth factors such as VEGF, or by disruption of the Bruch's membrane/retinal pigment epithelium complex with laser treatment. We wished to establish a transgenic murine model of age-related macular degeneration, in which the overexpression of VEGF by the retinal pigment epithelium induces choroidal neovascularization. A construct consisting of a tissue-specific murine retinal pigment epithelium promoter (RPE(65) promoter) coupled to murine VEGF(164) cDNA with a rabbit beta-globin-3' UTR was introduced into the genome of albino mice. Transgene mRNA was expressed in the retinal pigment epithelium at all ages peaking at 4 months. The expression of VEGF protein was increased in both the retinal pigment epithelium and choroid. An increase of intravascular adherent leukocytes and vessel leakage was observed. Histopathology revealed intrachoroidal neovascularization that did not penetrate through an intact Bruch's membrane. These results support the hypothesis that additional insults to the integrity of Bruch's membrane are required to induce growth of choroidal vessels into the subretinal space as seen in age-related macular degeneration. This model may be useful to screen for inhibitors of choroidal vessel growth.

Age Factors↗